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Bhat MH, Hajam YA, Neelam, Kumar R, Diksha. Microbial Diversity and Their Role in Human Health and Diseases. ROLE OF MICROBES IN SUSTAINABLE DEVELOPMENT 2023:1-33. [DOI: 10.1007/978-981-99-3126-2_1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/04/2025]
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Wu Y, Wang W, Yu Z, Yang K, Huang Z, Chen Z, Yan X, Hu H, Wang Z. Mushroom-brush transitional conformation of mucus-inert PEG coating improves co-delivery of oral liposome for intestinal metaplasia therapy. BIOMATERIALS ADVANCES 2022; 136:212798. [PMID: 35929326 DOI: 10.1016/j.bioadv.2022.212798] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 12/19/2021] [Revised: 04/05/2022] [Accepted: 04/07/2022] [Indexed: 06/15/2023]
Abstract
The blocking of gastric mucosal intestinal metaplasia (IM) has been considered to be the pivotal method to control the occurrence of gastric cancer. However, there is still a lack of effective therapeutic agent. Here, we developed mucus-penetrating liposome system by covering surface with polyethylene glycol (PEG) chains (hydrophilic and electroneutral mucus-inert material) to co-delivery candidate drugs combination. Then studied the impact on the transmucus performance of different conformations, which were constructed by controlling the density of PEG chains on the surface. The results showed that the particle size of 5%PEG-Lip was less than 120 nm, the polydispersity index was less than 0.3, and the surface potential tended to be neutral. The D value (long chain spacing) of 5% PEG-Lip was 3.25 nm, which was close to the RF value (diameter of spherical PEG long chain group without external force interference) of 3.44 nm, and the L value (extended length) was slightly larger than 3.44 nm. In this case, PEG showed mushroom-brush transitional conformation on the surface of liposomes. This conformation was not only promoted stable delivery, but also shielded the capture of mucus more favorably, leading to a more unrestricted transportation in mucus. The further in vivo experimental results demonstrated the rapid distribution of liposomes, which gradually appeared both in the superficial and deep glandular of mucosa and gland cells at 1 h and absorbed into the cell cytoplasm at 6 h. The 5% PEG-Lip with the mushroom-brush transitional configuration recalled abnormal organ index and improved inflammation and intestinal metaplasia. The modified PEG conformation assay presented here was more suitable for liposomes. This PEG-modified liposome system has potential of mucus-penetrating and provides a strategy for local treatment of gastric mucosal intestinal metaplasia.
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Affiliation(s)
- Yuyi Wu
- Key Laboratory of Standardization of Chinese Herbal Medicine, Ministry of Education, State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Wenjun Wang
- Key Laboratory of Standardization of Chinese Herbal Medicine, Ministry of Education, State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Ziwei Yu
- Key Laboratory of Standardization of Chinese Herbal Medicine, Ministry of Education, State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Ke Yang
- Key Laboratory of Standardization of Chinese Herbal Medicine, Ministry of Education, State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Zecheng Huang
- Key Laboratory of Standardization of Chinese Herbal Medicine, Ministry of Education, State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Ziqiang Chen
- Key Laboratory of Standardization of Chinese Herbal Medicine, Ministry of Education, State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Xiaomin Yan
- Key Laboratory of Standardization of Chinese Herbal Medicine, Ministry of Education, State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China
| | - Huiling Hu
- Key Laboratory of Standardization of Chinese Herbal Medicine, Ministry of Education, State Key Laboratory of Characteristic Chinese Medicine Resources in Southwest China, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, China.
| | - Zhanguo Wang
- Collaborative Innovation Laboratory of Metabonomics, Standard Research and Extension Base & Collaborative Innovation Center of Qiang Medicine, School of Medicine, Chengdu University, Chengdu, China.
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Role of Gastric Microorganisms Other than Helicobacter pylori in the Development and Treatment of Gastric Diseases. BIOMED RESEARCH INTERNATIONAL 2022; 2022:6263423. [PMID: 35321071 PMCID: PMC8938066 DOI: 10.1155/2022/6263423] [Citation(s) in RCA: 6] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 09/17/2021] [Revised: 12/02/2021] [Accepted: 02/18/2022] [Indexed: 12/15/2022]
Abstract
The microenvironment in the stomach is different from other digestive tracts, mainly because of the secretion of gastric acid and digestive enzymes, bile reflux, special mucus barrier, gastric peristalsis, and so on, which all contribute to the formation of antibacterial environment. Microecological disorders can lead to gastric immune disorders or lead to the decrease of dominant bacteria and the increase of the abundance and virulence of pathogenic microorganisms and then promote the occurrence of diseases. The body performs its immune function through innate and adaptive immunity and maintains microbial balance through the mechanism of immune homeostasis. Microecological imbalance can lead to the invasion of pathogenic microorganisms and damage mucosal barrier and immune system. The coexistence of gastric microorganisms (including viruses and fungi) may play a synergistic or antagonistic role in the pathogenesis of gastric diseases. Probiotics have the ability to compete with intestinal pathogens, increase the secretion of immunoglobulin A (IgA), stimulate the production of mucin, bacteriocin, and lactic acid, regulate the expression and secretion of cytokines, and regulate the growth of microbiota, which all have beneficial effects on the host microbial environment. At present, most studies focused on Helicobacter pylori, ignoring other stomach microbes and the overall stomach microecology. So, in this article, we reviewed advances in human gastric microecology, the relationship between gastric microecology and immunity or gastric diseases, and the treatment of probiotics in gastric diseases, in order to explore new area for further study of gastric microorganisms and treatment of gastric diseases.
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Bruno G, Rocco G, Zaccari P, Porowska B, Mascellino MT, Severi C. Helicobacter pylori Infection and Gastric Dysbiosis: Can Probiotics Administration Be Useful to Treat This Condition? THE CANADIAN JOURNAL OF INFECTIOUS DISEASES & MEDICAL MICROBIOLOGY = JOURNAL CANADIEN DES MALADIES INFECTIEUSES ET DE LA MICROBIOLOGIE MEDICALE 2018; 2018:6237239. [PMID: 30275917 PMCID: PMC6151681 DOI: 10.1155/2018/6237239] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 06/13/2018] [Accepted: 07/30/2018] [Indexed: 02/07/2023]
Abstract
Helicobacter pylori (Hp) is responsible for one of the most common infections in the world. The prevalence exceeds 50% of the population in developing countries, and approximately one-third of the adults are colonized in North Europe and North America. It is considered a major pathogenic agent of chronic gastritis, peptic ulcer, atrophic gastritis, gastric cancer, and mucosa-associated lymphoid tissue lymphoma (MALT). Hp colonization modifies the composition of gastric microbiota that could drive the development of gastric disorders. Currently, an emerging problem in Hp treatment is represented by the increasing rate of antimicrobial therapy resistance. In this context, the search for adjuvant agents can be very useful to overcome this issue and probiotics administration can represent a valid option. The aim of this review is to describe the gastric microbiota changes during Hp colonization, the mechanisms of action, and a possible role of probiotics in the treatment of this infection.
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Affiliation(s)
- Giovanni Bruno
- Department of Internal Medicine and Medical Specialties, Gastroenterology Unit, Sapienza University, Rome, Italy
| | - Giulia Rocco
- Department of Internal Medicine and Medical Specialties, Gastroenterology Unit, Sapienza University, Rome, Italy
| | - Piera Zaccari
- Department of Internal Medicine and Medical Specialties, Gastroenterology Unit, Sapienza University, Rome, Italy
| | - Barbara Porowska
- Department of Cardio-Thoracic, Vascular Surgery and Transplants, Sapienza University, Rome, Italy
| | | | - Carola Severi
- Department of Internal Medicine and Medical Specialties, Gastroenterology Unit, Sapienza University, Rome, Italy
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A slippery slope: On the origin, role and physiology of mucus. Adv Drug Deliv Rev 2018; 124:16-33. [PMID: 29108861 DOI: 10.1016/j.addr.2017.10.014] [Citation(s) in RCA: 117] [Impact Index Per Article: 16.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/25/2017] [Revised: 09/17/2017] [Accepted: 10/29/2017] [Indexed: 02/07/2023]
Abstract
The mucosa of the gastrointestinal tract, eyes, nose, lungs, cervix and vagina is lined by epithelium interspersed with mucus-secreting goblet cells, all of which contribute to their unique functions. This mucus provides an integral defence to the epithelium against noxious agents and pathogens. However, it can equally act as a barrier to drugs and delivery systems targeting epithelial passive and active transport mechanisms. This review highlights the various mucins expressed at different mucosal surfaces on the human body, and their role in creating a mucoid architecture to protect epithelia with specialized functions. Various factors compromising the barrier properties of mucus have been discussed, with an emphasis on how disease states and microbiota can alter the physical properties of mucus. For instance, Akkermansia muciniphila, a bacterium found in higher levels in the gut of lean individuals induces the production of a thickened gut mucus layer. The aims of this article are to elucidate the different physiological, biochemical and physical properties of bodily mucus, a keen appreciation of which will help circumvent the slippery slope of challenges faced in achieving effective mucosal drug and gene delivery.
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Mucoadhesive vs. mucopenetrating particulate drug delivery. Eur J Pharm Biopharm 2015; 98:76-89. [PMID: 26598207 DOI: 10.1016/j.ejpb.2015.11.003] [Citation(s) in RCA: 214] [Impact Index Per Article: 21.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/10/2015] [Revised: 10/22/2015] [Accepted: 11/09/2015] [Indexed: 02/04/2023]
Abstract
Mucus layer is a hydrophilic absorption barrier found in various regions of the body. The use of particulate delivery systems showed potential in drug delivery to mucosal membranes by either prolonging drug residence time at the absorption or target membrane or promoting permeation of particles across mucus gel layer to directly reach underlying epithelium. Mucoadhesive particles (MAP) are advantageous for delivering drug molecules to various mucosal membranes including eyes, oral cavity, bladder and vagina by prolonging drug residence time on those membranes. In contrast, a broader particle distribution and deeper penetration of the mucus gel layer are accomplished by mucopenetrating particles (MPP) especially in the gastrointestinal tract. Based on the available literature in particular dealing with in vivo results none of both systems (MAP and MPP) seems to be advantageous over the other. The choice of system primarily depends on the therapeutic target and peculiar properties of the target mucosa including thickness of the mucus gel layer, mucus turnover rate and water movement within the mucus. Future trends are heading in the direction of combining both systems to one i.e. mucoadhesive and mucopenetrating properties on the same particles.
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Kate V, Ananthakrishnan N, Tovey FI. Is Helicobacter pylori Infection the Primary Cause of Duodenal Ulceration or a Secondary Factor? A Review of the Evidence. Gastroenterol Res Pract 2013; 2013:425840. [PMID: 23606834 PMCID: PMC3623110 DOI: 10.1155/2013/425840] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/27/2013] [Accepted: 03/07/2013] [Indexed: 02/06/2023] Open
Abstract
Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication of H. pylori infection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. Against this concept there are issues that need explanation such as the reason why only a minority of infected persons develop duodenal ulceration when infection with H. pylori is widespread. There is evidence that H. pylori infection has been prevalent for several centuries, yet duodenal ulceration became common at the beginning of the twentieth century. The prevalence of duodenal ulceration is not higher in countries with a high prevalence of H. pylori infection. This paper debate puts forth the point of view of two groups of workers in this field whether H. pylori infection is the primary cause of duodenal ulcer disease or a secondary factor.
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Affiliation(s)
- Vikram Kate
- Department of General and Gastrointestinal Surgery, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry 605006, India
| | - N. Ananthakrishnan
- Mahatma Gandhi Medical College & Research Institute, Pondicherry 607402, India
| | - Frank I. Tovey
- Division of Surgery and Interventional Science, University College London, London W1W 7ET, UK
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Alvarez A, Ibiza S, Hernández C, Alvarez-Barrientos A, Esplugues JV, Calatayud S. Gastrin induces leukocyte-endothelial cell interactions in vivo and contributes to the inflammation caused by Helicobacter pylori. FASEB J 2006; 20:2396-8. [PMID: 17015411 DOI: 10.1096/fj.05-5696fje] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Abstract
Gastric mucosal inflammation causes hypergastrinemia, and gastrin receptors have been detected in several leukocyte types. We have analyzed whether gastrin affects the leukocyte-endothelial cell interactions in vivo by monitoring leukocyte rolling, adhesion, and emigration in rat mesenteric venules using intravital microscopy. Mesenteric superfusion with exogenous gastrin increased these processes in a concentration- and time-dependent manner, effects prevented by the cholecystokinin (CCK)-2 receptor antagonists (proglumide, L-365,260) but not by the CCK-1 receptor antagonist devazepide. A similar response was induced by exogenous CCK or endogenously released gastrin. CCK-2 receptors were localized in mesenteric macrophages and polymorphonuclear leukocytes. This effect of gastrin is not modulated by somatostatin and is independent of the endogenous release of histamine. To analyze whether hypergastrinemia elicited by Helicobacter pylori (HP) modulates the inflammation induced by the germ, rats were chronically administered with an extract of a CagA+/VacA+ strain of HP. This protocol increased gastrinemia and induced an inflammatory response in the rat mesentery. Blockade of CCK-2 receptors attenuated this response and induced a qualitative change in the leukocyte infiltrate suggestive of a receding inflammatory process. Our results reveal a new proinflammatory role of gastrin that seems to contribute to the maintenance of the inflammation elicited by HP components.
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Affiliation(s)
- Angeles Alvarez
- Departamento de Farmacología, Facultad de Medicina, Universidad de Valencia, Avd. Blasco Ibáñez 15, 46010-Valencia, Spain
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Fahey JW, Haristoy X, Dolan PM, Kensler TW, Scholtus I, Stephenson KK, Talalay P, Lozniewski A. Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains of Helicobacter pylori and prevents benzo[a]pyrene-induced stomach tumors. Proc Natl Acad Sci U S A 2002; 99:7610-5. [PMID: 12032331 PMCID: PMC124299 DOI: 10.1073/pnas.112203099] [Citation(s) in RCA: 519] [Impact Index Per Article: 22.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 04/05/2002] [Indexed: 02/06/2023] Open
Abstract
Gastric infection with Helicobacter pylori is a cosmopolitan problem, and is especially common in developing regions where there is also a high prevalence of gastric cancer. These infections are known to cause gastritis and peptic ulcers, and dramatically enhance the risk of gastric cancer. Eradication of this organism is an important medical goal that is complicated by the development of resistance to conventional antimicrobial agents and by the persistence of a low level reservoir of H. pylori within gastric epithelial cells. Moreover, economic and practical problems preclude widespread and intensive use of antibiotics in most developing regions. We have found that sulforaphane [(-)-1-isothiocyanato-(4R)-(methylsulfinyl)butane], an isothiocyanate abundant as its glucosinolate precursor in certain varieties of broccoli and broccoli sprouts, is a potent bacteriostatic agent against 3 reference strains and 45 clinical isolates of H. pylori [minimal inhibitory concentration (MIC) for 90% of the strains is
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Affiliation(s)
- Jed W Fahey
- Lewis B. and Dorothy Cullman Cancer Chemoprotection Center, Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205-2185, USA.
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Ricci V, Sommi P, Fiocca R, Necchi V, Romano M, Solcia E. Extracellular pH modulates Helicobacter pylori-induced vacuolation and VacA toxin internalization in human gastric epithelial cells. Biochem Biophys Res Commun 2002; 292:167-74. [PMID: 11890688 DOI: 10.1006/bbrc.2002.6638] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/14/2023]
Abstract
In this study we investigated whether an acidic extracellular pH may inhibit H. pylori-induced internalization of bacterial virulence factors by gastric epithelium, thus preventing ingestion of potentially dangerous luminal contents and resulting cellular damage. The interaction of H. pylori VacA toxin and ammonia (produced by H. pylori urease) with partly polarized gastric MKN 28 cells in culture was investigated at neutral and moderately acidic pH (6.2, compatible with cell viability) by means of neutral red dye uptake and ultrastructural immunocytochemistry. We found that acidic extracellular pH virtually abolished both VacA-dependent and ammonia-dependent cell vacuolation, as shown by the neutral red test, and caused a 50% decrease in VacA internalization into endosomal vesicles and vacuoles, as assessed by quantitation of immunogold particles. In addition, acidic pH blocked endosomal internalization of H. pylori outer membrane vesicles, a convenient indicator of endocytosis. Our data raise the possibility that suppression of gastric acid may increase H. pylori-induced gastric damage by enhancing epithelial internalization of H. pylori virulence factors through activation of endocytosis. Increased transmembrane diffusion of ammonia could also contribute to this process.
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Affiliation(s)
- Vittorio Ricci
- Institute of Human Physiology, University of Pavia and IRCCS Policlinico San Matteo, 27100 Pavia, Italy
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De Francesco V, Zullo A, Rinaldi V, Hassan C, Ballanti P, Winn S, Diana F, Morini S, Attili AF. Relationship between antral lymphocyte density and basal gastrin levels in patients with Helicobacter pylori infection. Dig Liver Dis 2000; 32:676-81. [PMID: 11142576 DOI: 10.1016/s1590-8658(00)80329-1] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
BACKGROUND The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood. AIM To evaluate whether antral lymphocyte density could play a role in this alteration. METHODS A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment. RESULTS Antral lymphocyte density (5,464 +/- 1,328 and 5,635 +/- 1,186 vs 2,267 +/- 557 lymphocytes/mm2; p<0.001 and p<0.001, respectively) and gastrin levels (66.7 +/- 14.1 and 60.4 +/- 21.7 vs 40.7 +/- 7.8 pg/dl; p=0.004 and p=0.02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and non-ulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0.77; p=0.003) and in non-ulcer dyspepsia (r=0.75; p=0.03) patients, while no correlation was found in controls [r=0.12; p=0.8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0.027), but disappeared in those successfully cured. CONCLUSIONS These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.
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Affiliation(s)
- V De Francesco
- Department of Clinical Medicine, Gastroenterology II, La Sapienza University, Rome, Italy
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Nijevitch AA. Helicobacter pylori-dependent intragastric urea biodegradation in children: diagnostic and pathogenetic importance. ACTA PAEDIATRICA JAPONICA : OVERSEAS EDITION 1998; 40:122-30. [PMID: 9581301 DOI: 10.1111/j.1442-200x.1998.tb01895.x] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/29/2022]
Abstract
The objective of the present work was to study the relationship between intragastric urea hydrolysis generated by Helicobacter pylori urease and acid-peptic disease in childhood. Intragastric urease activity was examined by urea and ammonia concentration measurement in gastric juice in 91 children with upper abdominal complaints. Helicobacter pylori infection was detected from 70 (76.9%) of 91 patients, including all of the 15 subjects with peptic ulcer disease. Helicobacter pylori-related gastritis in children was associated with a decrease of urea and an increase of ammonia in gastric juice (P < 0.001) in comparison with H. pylori-negative children. The gastritis score was correlated with the concentrations of urea and ammonia in the gastric juice of patients infected with H. pylori. There was a significant correlation between the histologically detected dissemination of organisms and gastric ammonia levels. Similar results were obtained concerning correlation between gastric juice ammonia and anti-H. pylori specific immunoglobulin G versus highly purified antigen of H. pylori containing urease. Present findings prove that H. pylori plays an essential role in the pathogenesis of gastritis and that ammonia is one of the main pathogenic factors of acid-peptic disease.
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Affiliation(s)
- A A Nijevitch
- Children's Republican Hospital, Bashkortostan, Ufa, Russia
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Fallone CA, Barkun AN, Göttke MU, Beech RN. A review of the possible bacterial determinants of clinical outcome inHelicobacter pyloriinfection. Can J Microbiol 1998. [DOI: 10.1139/w97-143] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
Helicobacter pylori is present in 40-60% of the population and approximately 10-20% of these infected individuals suffer from a H. pylori associated disease such as peptic ulcer disease or gastric cancer. This article reviews the potential bacterial determinants responsible for and markers predictive of both the acquisition of H. pylori infection and subsequent clinical outcome; i.e., asymptomatic infection or disease. The acquisition of H. pylori infection depends on exposure (hence the increased risk in lower socioeconomic groups and developing nations) to viable bacteria with at least a functional urease gene in a susceptible host. Once infection occurs, bacterial virulence factors, including the vacuolating cytotoxin, and genes of the cag pathogenicity island, as well as nonbacterial factors may determine disease outcome. Future research is being directed at discovering other bacterial virulence factors responsible for the different clinical outcomes of H. pylori infection. This will be greatly enhanced by the recent release of the complete genome sequence of H. pylori. The determination of the relative importance of each of these recognized and other as yet unrecognized factors responsible for disease outcome will assist in the appropriate targeting of patients in the treatment of H. pylori infection.Key words: Helicobacter pylori, genetics, virulence, bacterial.
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14
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Chen XQ, Zhang WD, Jiang B, Song YG, Reng RZ, Zhou DY. Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection. World J Gastroenterol 1997; 3:31-4. [PMID: 27006581 PMCID: PMC4796834 DOI: 10.3748/wjg.v3.i1.31] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/13/1996] [Revised: 10/01/1996] [Accepted: 01/01/1997] [Indexed: 02/06/2023] Open
Abstract
AIM: To investigate the concentration changes of epidermal growth factor (EGF) in duodenal ulcer patients with Helicobacter pylori (H. pylori) infection.
METHODS: Immunoreactive concentration of somatostatin, gastrin and epidermal growth factor of gastric and saliva juice in healthy volunteers, and chronic gastritis and duodenal ulcer patients with H. pylori infection were measured by radioimmunoassay.
RESULTS: Gastrin concentration of gastric juice in H. pylori-positive chronic gastritis (P > 0.05) and duodenal ulcer patients (P < 0.01) was higher than that of healthy volunteers (P < 0.05), whereas som atostatin concentration of gastric juice in chronic gastritis (P < 0.05) and duodenal ulcer patients (P < 0.01) was lower than that in healthy volunteers. Furthermore, EGF levels of gastric and saliva juice in duodenal ulcer patients with H. pylori infection (n = 10, 272.0 ng/L ± 96.3 ng/L and 8.3 ng/L ± 2.4 ng/L, respectively) were significantly lower than that in healthy volunteers (n = 12, 405.6 ng/L ± 35.6 ng/mL and 22.0 ng/L ± 17.0 ng/L, respectively) and in H. pylori-positive chronic gastritis patients (n = 25, 423.0 ng/L ± 104.0 ng/L and 22.0 ng/L ± 11.1 ng/L, respectively (P < 0.05).
CONCLUSION: A lower secretion of EGF may be a causative factor in the pathogenesis of H. pylori-positive duodenal ulcer.
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15
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Brooks MJ, Maxson CJ, Rubin W. The infectious etiology of peptic ulcer disease. Diagnosis and implications for therapy. Prim Care 1996; 23:443-54. [PMID: 8888337 DOI: 10.1016/s0095-4543(05)70340-7] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Abstract
During the past decade, peptic ulcer disease has become recognized as multifactorial in etiology, with a major component thought to be infection of the gastric mucosa with a spiral-shaped bacterium known as Helicobacter pylori. This organism has been found to cause most cases of chronic gastritis and is clearly pathogenic in most cases of duodenal and gastric ulceration. Biologic characteristics, epidemiology, and methods of detection (invasive and noninvasive) of H. pylori are discussed from a clinical perspective. Finally, eradication of H. pylori infection is difficult because of bacterial resistance and patient noncompliance.
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Affiliation(s)
- M J Brooks
- Department of Medicine, Allegheny University of the Health Sciences, Philadelphia, Pennsylvania, USA
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16
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Abstract
Research is asking how H. pylori causes diseases, and also why the same bacteria produces different conditions in different persons. The process involves bacterial factors and the host's response. Some bacterial factors such as urease are produced by all strains of H. pylori. This enzyme may damage the gastric epithelium by practically releasing ammonia. Other bacterial factors such as vacuolating toxin are only produced by some strains, and these strains are more likely to cause ulcers or cancer. The host's response has been studied by physiologists, immunologists, and histologists, but the separation of systems is artificial. For example, physiologists find that H. pylori stops gastric D-cells from expressing somatostatin normally, which impairs reflex inhibition of acid secretion, but the D-cell malfunction is probably due to inflammatory factors. In H. pylori gastritis, the gastric epithelial cells behave like immunocytes and express class II molecules and cytokines such as interleukin-8. The patient's histological response to H. pylori is quite closely related to the disease outcome. Patients who respond by developing gastric atrophy are more likely to get gastric ulcers or stomach cancer, but patients whose gastric corpus remains healthy tend to secrete more acid and develop duodenal ulcers, particularly if they have gastric metaplasia in their duodenum. Studies of disease mechanisms provide a valuable insight into the development of these common diseases, and may enable us to identify at-risk groups who particularly merit eradication therapy.
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Affiliation(s)
- J Calam
- Royal Postgraduate Medical School, Hammersmith Hospital, London, UK
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Clyne M, Labigne A, Drumm B. Helicobacter pylori requires an acidic environment to survive in the presence of urea. Infect Immun 1995; 63:1669-73. [PMID: 7729871 PMCID: PMC173208 DOI: 10.1128/iai.63.5.1669-1673.1995] [Citation(s) in RCA: 144] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/26/2023] Open
Abstract
The aim of this work was to study the significance of the urease enzyme in promoting Helicobacter pylori survival in various environments. A urease-positive H. pylori isolate, strain N6, and an isogenic urease-negative strain, strain N6(ureB::TnKm), were incubated in phosphate-buffered saline at a pH ranging from 2.2 to 7.2 for 60 min at 37 degrees C in both the presence and the absence of 10 mM urea. The number of CFU per milliliter in each solution, the pH of the bacterial supernatant, and the amounts of ammonia present in the solutions were measured. H. pylori N6 survived well in solutions with pH values ranging from 4.5 to 7.0 in the absence of urea but survived in solutions only with an initial pH below 3.5 in the presence of urea. Neither strain grew after incubation in an alkaline environment. The pH of an acidic solution (i.e., 3.5) rose rapidly to 8.45 in the presence of the wild-type strain and urea. The urease-negative mutant survived in solutions with pH values ranging from 4.5 to 7.2 irrespective of the presence of urea. Ammonia was present in significant amounts when H. pylori N6 was incubated in the presence of urea. Strain N6 survived exposure to concentrations of ammonia as high as 80 mM. The acid environment of the stomach may be crucial for H. pylori survival in the presence of urea. H. pylori does not survive in the normal environment in the presence of urea because of the subsequent rise in pH rather than ammonia toxicity.
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Affiliation(s)
- M Clyne
- Department of Paediatrics, University College Dublin, Our Lady's Hospital for Sick Children, Crumlin, Ireland
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